Phenotypes associated with this allele

• Allele Symbol: Ywhaq^{Gt(RRR746)Byg}
• Allele Name: gene trap RRR746, BayGenomics
• Allele ID: MGI:3700919
• Summary: 2 genotypes

Jump to	Allelic Composition	Genetic Background	Genotype ID
hm1	Ywhaq^Gt(RRR746)Byg/Ywhaq^Gt(RRR746)Byg	involves: 129P2/OlaHsd * C57BL/6	MGI:3702038
ht2	Ywhaq^Gt(RRR746)Byg/Ywhaq^+	involves: 129P2/OlaHsd * C57BL/6	MGI:3702039

Genotype
MGI:3702038

hm1

• Allelic Composition: Ywhaq^{Gt(RRR746)Byg}/Ywhaq^{Gt(RRR746)Byg}
• Genetic Background: involves: 129P2/OlaHsd * C57BL/6

• ♀: phenotype observed in females
• ♂: phenotype observed in males
• N: normal phenotype

mortality/aging

embryonic lethality during organogenesis, incomplete penetrance ( J:118280 )

• most embryos die by 14 days post-coitum; most die between 12 and 13 days post-coitum (dpc)

embryo

embryonic growth arrest ( J:118280 )

• 8- to 11-dpc embryos show signs of growth arrest

embryonic growth retardation ( J:118280 )

• most embryos examined at 8 and 11 dpc reveal generalized developmental delay

decreased embryo size ( J:118280 )

• at early stages, particularly 8 dpc, deciduae are smaller than wild-type

growth/size/body

embryonic growth retardation ( J:118280 )

• most embryos examined at 8 and 11 dpc reveal generalized developmental delay

decreased embryo size ( J:118280 )

• at early stages, particularly 8 dpc, deciduae are smaller than wild-type

cardiovascular system

cardiovascular system phenotype ( J:118280 )

N • embryos examined at 8 and 11 dpc do not show specific cardiac defects

Genotype
MGI:3702039

ht2

• Allelic Composition: Ywhaq^{Gt(RRR746)Byg}/Ywhaq⁺
• Genetic Background: involves: 129P2/OlaHsd * C57BL/6

mortality/aging

increased susceptibility to induced morbidity/mortality ( J:118280 )

• after myocardial infarction surgery, mutant mice show an increased mortality rate over 7 days following surgery; only 7/17 mutants survive 7 days compared to 11/15 wild-type

embryo

embryonic growth retardation ( J:118280 )

• most embryos examined at 8 and 11 dpc reveal generalized developmental delay

growth/size/body

embryonic growth retardation ( J:118280 )

• most embryos examined at 8 and 11 dpc reveal generalized developmental delay

cardiovascular system

cardiovascular system phenotype ( J:118280 )

N • at 12 weeks, mice do not show notable cardiac morphological or functional differences from wild-type

abnormal heart ventricle morphology ( J:118280 )

• after myocardial infarction surgery, mice that die uniformly show ventricular free wall rupture

dilated heart left ventricle ( J:118280 )

• 1 week after myocardial infarction surgery, mutant mice show marked left ventricular dilatation compared to wild-type

abnormal cardiovascular system physiology ( J:118280 )

• end diastolic volume and end systolic volume are increased in mutants at 1 week post myocardial infarction surgery

increased cardiomyocyte apoptosis ( J:118280 )

• cultured cardiomyocytes show an ~8-fold increased rate of apoptosis in response to UV-C irradiation

• apoptosis across the infarct border zones is greater in mutant tissue than in wild-type

increased myocardial infarct size ( J:118280 )

• 7 days after left coronary artery ligation, infarction size is significantly greater in mutants (48% of left ventricular area vs 32% in wild-type)

muscle

increased cardiomyocyte apoptosis ( J:118280 )

• cultured cardiomyocytes show an ~8-fold increased rate of apoptosis in response to UV-C irradiation

• apoptosis across the infarct border zones is greater in mutant tissue than in wild-type

homeostasis/metabolism

increased myocardial infarct size ( J:118280 )

• 7 days after left coronary artery ligation, infarction size is significantly greater in mutants (48% of left ventricular area vs 32% in wild-type)

abnormal enzyme/coenzyme activity ( J:118280 )

• JNK and P38 MAPK activity is greater in mutant heart tissue

cellular

increased cardiomyocyte apoptosis ( J:118280 )

• cultured cardiomyocytes show an ~8-fold increased rate of apoptosis in response to UV-C irradiation

• apoptosis across the infarct border zones is greater in mutant tissue than in wild-type